Unusual cause of desynchronization in a cardiac resynchronization device.

This report describes a new cause of desynchronization encountered in a cardiac resynchronization device functioning in the VVIR mode. Left ventricular stimulation was inhibited when the sensor-driven rate exceeded the programmed left ventricular (LV) maximum trigger rate. With these devices, it is important to program the LV maximum trigger interval (essentially equivalent to a LV upper interval) to a value equal or faster than the sensor-driven upper rate.

P-wave locking in the postventricular atrial refractory period of cardiac resynchronization devices. Management with the Biotronik system.

Electrical desynchronization in cardiac resynchronization therapy (CRT) occurs when sinus P waves are continually locked in the postventricular atrial refractory period (PVARP). This process is characterized by sequences of a P wave as an atrial event in the PVARP followed by a conducted and sensed ventricular event. Such sequences are more common in patients with a prolonged PR interval, often initiated by premature ventricular complexes (PVC) and terminated by PVCs or slowing of the sinus rate. Specific algorithms automatically identify a recurring pattern of P wave locking in the PVARP, whereupon they shorten the PVARP temporarily until atrial tracking is restored with the programmed sensed AV interval. The Biotronik family of Lumax CRT devices use an AV control window which is not an algorithm that "unlocks" P waves trapped in the PVARP. Rather, it prevents P waves from becoming trapped in the PVARP. A ventricular sensed event occurring within the AV control interval does not start a PVARP so that P wave locking cannot occur when the AV conduction time is shorter than the AV control interval.

Using devices with a variable postventricular atrial refractory period for cardiac resynchronization.

Automatic postventricular atrial refractory period (Auto-PVARP) is a dynamic interval designed to provide a longer PVARP at slower rates to enhance protection against pacemaker tachycardia (PMT) and a shorter PVARP to enhance atrial sensing at high rates. Auto-PVARP is often programmed in Medtronic devices for cardiac resynchronization therapy (CRT) with little knowledge of its intricate manifestations and disadvantages. The use of Auto-PVARP is contradictory to the universal teaching that CRT devices should be programmed with a short PVARP. We present the sequential ECGs of a patient with a CRT device programmed with Auto-PVARP in whom the atrial rate was increased with isoproterenol to simulate exercise. The recordings demonstrated that Auto-PVARP produced a substantial delay in the restoration of AV synchrony from the time the spontaneous atrial rate dropped below the programmed upper tracking rate. Auto-PVARP makes little sense (especially in the presence of first-degree AV block) in CRT patients considering that PMT is rare in this situation. In CRT patients, one should program a short and fixed PVARP of ≤ 250 ms.

Impact of increasing current drain in a pacemaker operating during activation of the elective replacement indicator.

The occurrence of a 13.8 s episode of ventricular asystole in a patient whose VVIR pacemaker displayed the elective replacement indicator (ERI) is reported. Increasing battery current drain by VARIO testing and programming of the emergency VVI mode markedly increased battery current drain with a resultant decrease in the battery voltage below the pacing threshold. The prolonged lack of capture occurred because the lowered battery voltage could not return instantaneously to its previous level after the demand for a higher battery current drain had ceased. Rather, the battery voltage increased progressively to its previous level and successful capture was eventually regained at the previous base rate. When a pacemaker is at or near the ERI point, it is important to avoid any manipulation (including VARIO testing) that increases battery current drain so as to prevent prolonged ventricular asystole in pacemaker-dependent patients.

A reappraisal of pacemaker timing cycles pertaining to automatic mode switching.

Automatic mode switching algorithms of dual chamber pacemakers require fundamental changes in the operation of pacemaker timing cycles to optimize detection of supraventricular tachyarrhythmias. The timing cycles related to mode switching are basically independent of the algorithm design. Blanking periods (when the sensing amplifier is temporarily disabled) should be optimized to a relatively small fraction of the pacing cycle to enhance atrial sensing and prevent far-field sensing. This review explains the function of the timing cycles pertaining to mode switching and proposes simpler terminology to facilitate the understanding of pacemaker function and electrographic interpretation of complex recordings.

Rate adaptive dual chamber pacing: inappropriate rate response due to pseudomalfunction of the QT biosensor.

Inappropriate tachycardias may be observed in patients with DDDR pacemakers equipped with an activity sensor and a QT sensor due erroneous T wave sensing, provoked by drug treatment that prolongs cardiac repolarization.

Left posterior fascicular tachycardia: a diagnostic and therapeutic challenge.

A wide QRS complex tachycardia with right bundle-branch block morphology and left axis deviation observed in a young patient without structural heart disease may pose a diagnostic and therapeutic challenge. The surface ECG may provide several diagnostic clues to make a correct diagnosis of left posterior fascicular tachycardia and may help to differentiate it from both a supraventricular tachycardia with aberrant conduction and a typical ventricular tachycardia related to coronary artery disease. Although this tachycardia is sensitive to verapamil, this medication may probably cause transient infertility in males. The presence of a Purkinje potential preceding the QRS complex during tachycardia and optimal pace mapping may guide radio-frequency ablation resulting in a definite cure.

Implantable Holter may reveal cause of unexplained syncope.

A definitive diagnosis in patients with syncope is often problematic if the cause is not evident after initial clinical assessment. The cause of syncope may be not established due to the infrequent, episodic occurrence. A symptom-rhythm correlation is frequently an unattainable gold standard in many patients. The implantable Holter has added a powerful tool to the diagnostic armamentarium in the field of arrhythmia detection and may assume a prominent role in the investigation of syncope.

Propafenone for conversion and prophylaxis of atrial fibrillation. Propafenone Atrial Fibrillation Trial Investigators.

Pharmacologic therapy is widely used for restoration of sinus rhythm and prevention of recurrences of atrial fibrillation. Because concerns have been raised about their potential proarrhythmic effects, therapeutic regimens should be evaluated by placebo-controlled studies to determine their efficacy and safety. One hundred thirty-six patients with persistent atrial fibrillation were randomized to receive propafenone 2 mg/kg over 30 minutes, followed by oral propafenone 150 mg 3 times daily or matching placebo. Nonresponders to intravenous therapy underwent direct-current cardioversion. Both responders to intravenous therapy and converters to sinus rhythm after direct-current cardioversion were followed for 6 months in a double-blind oral treatment period of propafenone 150 mg 3 times daily or matching placebo. Pharmacologic conversion to sinus rhythm was achieved in 29% of the patients taking propafenone and in 17% of patients taking placebo (p > or = 0.10). Subsequent direct-current cardioversion in nonresponders was equally successful (70%) in both groups (p > or = 0.10). The proportion of patients free from recurrent symptomatic arrhythmia at 6 months was 67% for the propafenone and 35% for the placebo group (p < 0.01). Time to atrial fibrillation relapse was more favorable with propafenone than with placebo (p < 0.001). The incidence of drug-related side effects was 10% in the propafenone group and 14% in the placebo group. Thus, "slow" infusion of propafenone seems to be of limited value for terminating atrial fibrillation. Oral propafenone at a low dosage 150 mg 3 times daily is well tolerated and effective in maintaining sinus rhythm for 6 months after pharmacologic or electrical restoration of sinus rhythm.

Review of the reviewer.

Reviewers can disagree substantially when evaluating the same materials. For papers submitted to an editorial board, the Editor-in-Chief can suggest compromises. However, this is not the case in the normal abstract grading procedures for large meetings. If important discrepancies arise between reviewers, a review committee may propose corrective measures. However, this is only feasible for smaller meetings with a limited number of abstract submissions. In this study, when reviewing the same abstracts, a statistically significant correlation between reviewers was present in 15 instances and absent in 13 others. It would appear that some review of the reviewer is highly desirable and may prevent publication bias.

Biophysical and electrical aspects of radiofrequency catheter ablation.

UNLABELLED: Radiofrequency (RF) catheter ablation is becoming increasingly accepted as the treatment of choice for definitive management of a variety of supraventricular arrhythmias in selected patients. Many interdependent variables may affect the amount of tissue heating at the target site. Power controlled RF devices may fail to ablate the targeted tissue due to a mismatch between the actual resistance of the electrode-tissue interface and the internal resistance of the RF generator. CONCLUSION: the use of temperature controlled RF devices may optimize power delivery to the tissue and therefore facilitate radiofrequency catheter ablation procedures.

Voltage dip in pacemaker battery supply: a new cause of pacemaker mediated tachycardia.

A new cause of pacemaker mediated tachycardia was observed in a patient equipped with a Vitatron Quintech 931 DDD pacemaker. In this type of pacemaker the microprocessor is switched off during the atrial refractory period. Beyond the recommended replacement time, the internal resistance of the battery may increase to such an extent that switching on and off the microprocessor may cause voltage dips. Those voltage dips are erroneously interpreted as P waves by the atrial sensing amplifier, which may cause self-triggering of the pacemaker and initiate a pacemaker mediated tachycardia.

Efficacy and safety of intravenous sotalol for termination of paroxysmal supraventricular tachycardia. The Sotalol Versus Placebo Multicenter Study Group.

A double-blind, placebo-controlled, crossover, multicenter study was conducted to study the efficacy and safety of a single intravenous dose of sotalol (1.5 mg/kg over 10 minutes) in achieving normal sinus rhythm in paroxysmal supraventricular tachycardia (SVT) lasting greater than or equal to 15 minutes. Patients were randomized to either sotalol or placebo as initial treatment, and if the SVT was not terminated a crossover was performed after 20 minutes. A total of 43 patients were enrolled, 38 of whom with spontaneous (n = 14) or induced (n = 24) SVT were analyzed for sotalol efficacy. Most patients (n = 27) had atrioventricular (AV) nodal reentrant tachycardia, and an important subgroup (n = 11) had circus movement tachycardia, using an accessory pathway for retrograde conduction. The number of patients converting to sinus rhythm as a result of the initial treatment was significantly higher in the sotalol group than in the placebo group, for spontaneous (p less than 0.005) as well as for induced tachycardia (p less than 0.001). Sinus rhythm was achieved within 30 minutes in 83% of all patients who received sotalol as the first drug, compared with 16% of the patients first receiving placebo (p less than 0.0001). For sotalol safety analysis, 42 patients were included. A total of 37 patients received sotalol, 19 as the first treatment, and 18 as the second treatment, while 25 patients received placebo. A total of 15 possible adverse effects were reported, occurring in 10 patients with sotalol versus 4 with placebo. The only severe side effect (hypotension) necessitating termination of drug administration occurred with placebo. No proarrhythmic effects were observed.(ABSTRACT TRUNCATED AT 250 WORDS)

Effect of the infusion of magnesium sulfate during atrial pacing on ECG intervals, serum electrolytes, and blood pressure.

Magnesium salts have been used for decades for the empiric treatment of arrhythmias, particularly torsades de pointes, associated with long QT syndrome. The mechanism underlying this antiarrhythmic effect is still not clear. Therefore the effect of intravenous MgSO4 on serum electrolytes, blood pressure, and ECG variables was evaluated in nine patients with sick sinus syndrome, equipped with a DDD pulse generator, programmed in the atrial asynchronous mode. A total dose of 10 gm MgSO4 was given intravenously over 6 hours at a constant rate. Blood pressure and serum electrolytes were determined before (t0), 3 hours after (t3), and at the end of the magnesium infusion (t6). ECG variables were measured at t0, t3, and t6 at different pacing frequencies (60, 80, and 100 beats/min). Serum magnesium levels rose significantly from 0.88 mmol.l-1 at t0 to 1.91 mmol.l-1 at t6 (p less than 0.05). Magnesium infusion did not affect blood pressure, pulse rate, PR or QRS or QT interval. Increasing the pacing frequency resulted in a statistically significant QT shortening at each serum magnesium level. We conclude that intravenous magnesium administration does not influence the QT interval. Increasing atrial pacing rate shortens the QT interval and this QT shortening is not affected by magnesium. Sustained serum magnesium levels between 1.5 and 2 mmol.l-1 are hemodynamically well tolerated and do not give rise to the development of higher degree atrioventricular block.

The superfast atrial recharge pulse: a cause of pectoral muscle stimulation in patients equipped with a unipolar DDD pacemaker.

Pectoral muscle stimulation may cause serious discomfort to patients equipped with a pulse generator. Insulation defects of the lead, connector problems and defective coating of the pacemaker can are common causes of local muscle contractions. This report describes pectoral muscle stimulation caused by the atrial superfast recharge pulse incorporated into the atrial channel of a commercially available unipolar DDD pacemaker. As pectoral muscle stimulation could not be eliminated by reprogramming the pacemaker to a lower atrial output in some patients a redesign of the pacemaker is highly required.

Delayed elimination of digoxin antidotum determined by radioimmunoassay.

An observation of a treatment with digitalis antibodies (Fab-fragments) in a young child is presented. The elimination of this antidotum proved to be much slower than normally expected. In the patient's history, the disappearance of the Fab-fragments out of the blood lasted 142 days with a half-life of 15.6 days, whereas an elimination with a T1/2 of 28 hours is accepted. Probably there has been intracellular penetration of the antibodies into the liver, caused by concomitant diseases (Hepatitis A and B infections). An "in vitro" experiment is reported. It demonstrates the equimolar binding of the Fab-fragments for digoxin and shows that the elimination of the Fab-fragments can be established by a routine radioimmunoassay of digoxin, in an indirect way.

Sodium channel block by a potent, new antiarrhythmic agent, transcainide, in guinea pig ventricular myocytes.

Transcainide is a new lidocaine analog that has been shown to suppress a range of cardiac arrhythmias in an initial clinical trial. We have evaluated the effects of transcainide on sodium channel current in guinea pig ventricular myocytes using the whole-cell patch-clamp technique. Reduction of sodium current by transcainide was concentration dependent, with an ED50 of approximately 0.5 microM (n = 9). This reduction of the sodium current exhibited little use dependence, and block did not accumulate even after 10-Hz pulse trains. Moreover, little or no recovery from block was observed even when cells were hyperpolarized to -160 mV for 1 min. We observed no reversal of sodium channel block after superfusing cells up to 1 h in drug-free solution. Thus, transcainide, unlike many other clinically useful antiarrhythmic agents, blocked sodium channels with very little time dependence or voltage dependence. These novel electrophysiological properties of transcainide may endow the agent with a unique spectrum of efficacy against certain arrhythmias. At the same time, the great potency of transcainide and its lack of reversibility, at least within an hour, mandate that the drug should be used with great caution.

Pacing and sensing: how can one electrode fulfill both requirements?

Pacing and sensing are two different functions which can be accomplished by one and the same electrode. Optimal pacing requires a high tissue resistance in order to minimize the stimulation energy, making a small surface electrode highly desirable. For adequate sensing, however, the tissue resistance should be as low as possible which requires a larger electrode surface area. Decreasing the electrode surface area results in an increased polarization impedance. As this latter should be low for both pacing and sensing, an electrode with a large surface area should be used. How can these opposing needs be met by one electrode? The combination of a small geometrical surface and a large porous microstructure along with the choice of low polarizable materials meets both the requirements of pacing and sensing.

Effects of intravenous sotalol, aprindine and the combination of sotalol and aprindine on chronic high frequency ventricular arrhythmias in man.

The comparative antiarrhythmic efficacy of three different intravenous drug regimens was evaluated in 12 symptomatic patients (mean age: 72 years) with chronic high frequency ventricular arrhythmias (mean: 834 PVCs h-1). In a cross-over study with latin square distribution the following drug regimens were administered intravenously to all patients aprindine 2 mg kg-1, sotalol 1.5 mg kg-1, aprindine 1 mg kg-1 & sotalol 0.75 mg kg-1. The mean percentage of PVC reduction was 41% (P less than 0.05) for aprindine 2 mg kg-1; 51% (P less than 0.05) for sotalol 1.5 mg kg-1 and 72% (P less than 0.01) for the combined drug therapy (aprindine 1 mg kg-1 and sotalol 0.75 mg kg-1). The mean plasma concentration was 1371 ng ml-1 after administration of aprindine 2 mg kg-1 and 1730 ng ml-1 after infusion of sotalol 1.5 mg kg-1. After combined drug therapy, mean plasma levels were 942 ng ml-1 for aprindine and 992 ng ml-1 for sotalol. The different drug regimens were well tolerated in all patients and no side-effects occurred. Combination therapy consisting of a drug that prolongs action potential duration with an antiarrhythmic agent that has a high affinity for the inactivated channels may thus achieve an antiarrhythmic efficacy comparable to single agent therapy, permitting the use of lower dosages.